Trichoderma koningii and Trichoderma koningiopsis presented a global fungal core
community [15]. In the rhizosphere, Trichoderma species release constitutively
a blend rich in secondary metabolites that are involved in the different plant
beneficial effects that take part in the rhizosphere [7]. Figure 1 shows a metabolomic
profile of T. virens (Gv29-8) obtained by GC-MS, which illustrates the richness and
abundance of low molecular weight compounds.
Trichoderma spp. compounds include non-ribosomal peptides (NRPs),
siderophores, anthraquinones, daucanes, pyrones, koninginins, trichodermamides,
viridins, viridiofungins, nitrogen heterocyclic compounds, trichodenones and
cyclopentenone derivatives, acoranes, azaphilones, harzialactones and derivatives,
butenolides, trichothecenes, isocyano compounds, setin-like metabolites,
bisorbicillinoids, diketopiperazines, ergosterol derivates, peptaibols, cyclonerodiol
derivates, statins, koningic acid (heptelidic acid), and derivates [16].
Some compounds can promote plant growth, and others activate systemic resistance against plant pathogens. In the Trichoderma-plant interactions, it has been
observed important changes in the modulation of fungal enzymes that participate
in the biosynthesis of secondary metabolites. For example, T. virens Gv29-8 encodes
the gene TvCyt2 (a homologous protein of the p450 monooxygenase) that is
downregulated at the beginning of the fungal-plant interaction. GC-MS analysis
revealed that TvCyt2 is involved in the production of the compounds
viridiflorol, tau-muurolol, and α-cadinol and pyrazine [1,2-a] indole-1, 4-diene,
2,3-dihydro-2-methyl-3-methylene, and those compounds triggered plant defense
responses [17].
When Trichoderma interact with plant roots, it causes profound and substantial
changes at the biochemical level, which, depending on the kind of metabolite
regulated in planta, affect plant physiology, defense, and stress responses [18–21].
In plant tissues considerable changes in the phytohormone content after
Trichoderma spp. inoculation have been detected [22, 23]. In the case of melon
plants (Cucumis melo) inoculated with T. harzianum, significant increases in
the contents of zeatin, indole-3-acetic acid (IAA), abscisic acid (ABA),
1-aminocyclopropane-1-carboxylic acid (ACC, an ethylene precursor), jasmonic
acid (JA), and salicylic acid (SA) were detected in the shoot [24]. Figure 2a, b
shows the growth pattern of Arabidopsis thaliana in control and T. virens-inoculated
plants, respectively. Root growth promotion was correlated with the increased
expression of the gene CycB1::GUS, a reporter of the cell division in the phase
G2/M of the cell cycle (Fig. 2c, f). Here, inoculated plants presented a phenotype
that resembles the effects induced by the plant growth regulator auxin (IAA) [11].
In fact, the content of phytohormones modulated by Trichoderma spp. in melon
plants is directly related with their phenotype [25].
2.1
Trichoderma Root Colonization
In the beginning of the Trichoderma-root interaction, plants under different
environmental conditions (stressed or non-stressed) release signaling molecules
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H. A. Contreras-Cornejo et al.
community [15]. In the rhizosphere, Trichoderma species release constitutively
a blend rich in secondary metabolites that are involved in the different plant
beneficial effects that take part in the rhizosphere [7]. Figure 1 shows a metabolomic
profile of T. virens (Gv29-8) obtained by GC-MS, which illustrates the richness and
abundance of low molecular weight compounds.
Trichoderma spp. compounds include non-ribosomal peptides (NRPs),
siderophores, anthraquinones, daucanes, pyrones, koninginins, trichodermamides,
viridins, viridiofungins, nitrogen heterocyclic compounds, trichodenones and
cyclopentenone derivatives, acoranes, azaphilones, harzialactones and derivatives,
butenolides, trichothecenes, isocyano compounds, setin-like metabolites,
bisorbicillinoids, diketopiperazines, ergosterol derivates, peptaibols, cyclonerodiol
derivates, statins, koningic acid (heptelidic acid), and derivates [16].
Some compounds can promote plant growth, and others activate systemic resistance against plant pathogens. In the Trichoderma-plant interactions, it has been
observed important changes in the modulation of fungal enzymes that participate
in the biosynthesis of secondary metabolites. For example, T. virens Gv29-8 encodes
the gene TvCyt2 (a homologous protein of the p450 monooxygenase) that is
downregulated at the beginning of the fungal-plant interaction. GC-MS analysis
revealed that TvCyt2 is involved in the production of the compounds
viridiflorol, tau-muurolol, and α-cadinol and pyrazine [1,2-a] indole-1, 4-diene,
2,3-dihydro-2-methyl-3-methylene, and those compounds triggered plant defense
responses [17].
When Trichoderma interact with plant roots, it causes profound and substantial
changes at the biochemical level, which, depending on the kind of metabolite
regulated in planta, affect plant physiology, defense, and stress responses [18–21].
In plant tissues considerable changes in the phytohormone content after
Trichoderma spp. inoculation have been detected [22, 23]. In the case of melon
plants (Cucumis melo) inoculated with T. harzianum, significant increases in
the contents of zeatin, indole-3-acetic acid (IAA), abscisic acid (ABA),
1-aminocyclopropane-1-carboxylic acid (ACC, an ethylene precursor), jasmonic
acid (JA), and salicylic acid (SA) were detected in the shoot [24]. Figure 2a, b
shows the growth pattern of Arabidopsis thaliana in control and T. virens-inoculated
plants, respectively. Root growth promotion was correlated with the increased
expression of the gene CycB1::GUS, a reporter of the cell division in the phase
G2/M of the cell cycle (Fig. 2c, f). Here, inoculated plants presented a phenotype
that resembles the effects induced by the plant growth regulator auxin (IAA) [11].
In fact, the content of phytohormones modulated by Trichoderma spp. in melon
plants is directly related with their phenotype [25].
2.1
Trichoderma Root Colonization
In the beginning of the Trichoderma-root interaction, plants under different
environmental conditions (stressed or non-stressed) release signaling molecules
266
H. A. Contreras-Cornejo et al.